Ks. Hsu et Sy. Linshiau, RELAXATION OF RAT THORACIC AORTA INDUCED BY PYRIDINE, European journal of pharmacology. Environmental toxicology and pharmacology section, 292(3-4), 1995, pp. 265-270
The pharmacological and toxicological activity of pyridine was determi
ned in rat thoracic aorta. Pyridine inhibited norepinephrine (3 mu M)-
induced phasic and tonic contractions in the thoracic aorta as well as
the endothelium-denuded aorta of the rat. The tonic pre-contraction e
licited by norepinephrine was also relaxed by the addition of pyridine
and this relaxing effect was not affected by indomethacin (20 mu M),
N-G-monomethyl-L-arginine acetate (50 mu M) or methylene blue (50 mu M
). In high-K+ medium (80 mM), pyridine inhibited the Ca2+ concentratio
n-dependent vasocontraction. Moreover, in Ca2+-free medium, the norepi
nephrine (3 mu M)-induced phasic contraction was also suppressed by py
ridine, while the caffeine (10 mM)-induced contraction remained unaffe
cted. The cAMP and cGMP levels of rat aorta were not changed by pyridi
ne. The Ca-45(2+) influx elicited by either norepinephrine or high-Kwas inhibited by pyridine in a concentration-dependent manner. All of
these findings indicated that pyridine relaxes rat thoracic aorta by v
irtue of its Ca2+ channel-blocking properties in vascular smooth muscl
e.